The core problem is deceptively straightforward. Fluid administration remains a cornerstone of resuscitating circulatory shock, yet only a subset of critically ill patients actually increases their stroke volume after a fluid bolus. For everyone else, the extra volume does nothing for the heart and everything for the wrong places: it pools in the lungs as pulmonary oedema, distends the systemic veins, and quietly damages organs through congestion. The traditional triggers for giving more fluid — hypotension, low urine output, a low central venous pressure — have been repeatedly discredited as predictors of who will benefit. What has emerged instead is a physiology-based framework in which each bolus must be justified twice over: once by evidence that the heart is preload responsive, and once by evidence that the body can absorb the added volume without harm.

Echocardiography occupies a unique position in this framework because it answers several clinically decisive questions within minutes at the bedside. It can identify pericardial tamponade, severe left or right ventricular dysfunction, acute cor pulmonale, major valvular disease, and septic cardiomyopathy. It can estimate whether additional fluid is likely to augment stroke volume, and it can detect signs that a patient is unlikely to tolerate more volume. But the review is emphatic about two caveats. First, a single snapshot is insufficient: echocardiography enables effective haemodynamic monitoring only when assessments are performed serially and frequently, because critically ill patients can deteriorate or improve within hours. Second, in the most severe or haemodynamically complex patients, echocardiography cannot replace continuous cardiac output monitoring, which clinical guidelines still recommend. The two tools are complementary rather than interchangeable — continuous monitors provide high-frequency haemodynamic trends, while echocardiography delivers anatomical and functional information, including valvular regurgitation, right ventricular function, and venous congestion patterns such as the Venous Excess Ultrasound score, that pulse-contour or thermodilution devices simply cannot see.

Static echocardiographic measurements — chamber size, inferior vena cava dimensions, diastolic indices — remain clinically valuable, but mostly because they describe the haemodynamic context rather than predict the effect of a future bolus. A small, hyperdynamic left ventricle may suggest fluid responsiveness, whereas a dilated, poorly contractile ventricle should raise immediate concern about fluid intolerance. The inferior vena cava is the most widely used bedside index because it is rapidly obtainable, yet its behaviour is confounded by spontaneous inspiratory effort, tidal volume, positive end-expiratory pressure, abdominal pressure, obesity, and even probe position. Reported diagnostic performance varies so widely across studies and ventilation conditions that IVC metrics should never be used in isolation to decide on fluid administration. Diastolic indices such as the E/e’ ratio and left atrial size are better understood as markers of filling pressure and fluid tolerance than as predictors of responsiveness — observational studies link an elevated E/e’ to higher left-sided filling pressures and poorer fluid tolerance, but its ability to predict whether stroke volume will rise has never been established in original research.

The real strength of echocardiography in fluid management lies in tracking changes in stroke volume surrogates during a controlled preload-modifying manoeuvre, and the workhorse measurement here is the left ventricular outflow tract velocity-time integral, or LVOT VTI. Pulsed-wave Doppler interrogation of the outflow tract yields a surrogate that can be measured repeatedly at the bedside; although absolute stroke volume calculation requires accurate LVOT diameter measurement, relative changes in VTI are more reproducible for serial decision-making. The technique is not without pitfalls. Subaortic VTI is susceptible to variability in angle correction, sample volume positioning, and signal quality, and small measurement errors can meaningfully distort the calculated change in cardiac output during a responsiveness test. This is formalised through the concept of the least significant change — the smallest change exceeding inherent measurement variability that can be interpreted as a true haemodynamic shift rather than random noise. For transthoracic LVOT VTI, studies estimate the least significant change at roughly 10 to 15 percent, which substantially overlaps with the diagnostic thresholds of around 5 to 10 percent commonly used for the end-expiratory occlusion test and the mini-fluid challenge. Some changes classified as diagnostic by these tests may therefore approach, or even fall within, the measurement noise of the technique itself — a sobering caveat that argues for averaged, repeated measurements and, in selected settings where the expected VTI change is small, for transoesophageal echocardiography with its greater image stability, balanced against its invasiveness.

Against this backdrop, one strategy stands out as the best validated: passive leg raising combined with real-time LVOT VTI measurement. Passive leg raising works by transferring venous blood from the legs and splanchnic circulation to the central compartment, producing a reversible endogenous fluid challenge without administering a single millilitre of intravenous fluid. When paired with real-time VTI monitoring, it achieves a pooled sensitivity of around 85 percent and a specificity of around 91 percent when preload responsiveness is assessed with any cardiac output monitoring technique, and it remains applicable in spontaneously breathing patients, mechanically ventilated patients, and those with arrhythmias — situations where most other dynamic indices fail. The procedural details matter enormously. The manoeuvre should move the patient from semi-recumbent to supine while simultaneously elevating the legs, preferably using the bed mechanism rather than manual lifting, with minimal patient stimulation and real-time capture of the maximal haemodynamic response. The response must be assessed with VTI rather than heart rate or blood pressure, which are insensitive and non-specific markers of preload-induced changes. VTI should be averaged over three to five cardiac cycles in sinus rhythm and up to ten to twelve cycles in arrhythmia. The commonly used threshold is a VTI increase of at least 10 to 12 percent within one minute of leg elevation, though some studies have used 15 percent. Passive leg raising is contraindicated or unreliable in intra-abdominal hypertension, elevated intracranial pressure, and morbid obesity, where the manoeuvre may fail to generate an effective preload challenge.

Two alternatives extend the approach when passive leg raising is impractical. The mini-fluid challenge administers a small bolus of 100 to 150 millilitres while the operator immediately reassesses LVOT VTI, achieving a sensitivity of roughly 82 percent and specificity of 83 percent; its main drawback is that some fluid is still given to non-responders, and repeated testing can cumulatively contribute to overload. The end-expiratory occlusion test, which transiently interrupts the ventilator circuit at end-expiration to increase cardiac preload without delivering fluid, performs even better on paper — sensitivity around 86 percent and specificity around 91 percent — but requires controlled mechanical ventilation without significant spontaneous effort, close bedside coordination, and real-time Doppler acquisition during a short time window. Respiratory variation in LVOT VTI, once a mainstay of ventilated patients, has fared worse: its specificity drops markedly in the largest multicentre cohort compared with earlier small studies, and its usefulness collapses under lung-protective ventilation, arrhythmias, right ventricular dysfunction, or altered thoraco-pulmonary compliance — which is precisely why contemporary practice increasingly favours functional tests over passive respiratory variation alone.

The most consequential conceptual shift in the review is the move from fluid responsiveness to fluid tolerance. A patient may still show a positive preload-responsiveness test while simultaneously exhibiting worsening lung ultrasound B-lines, venous Doppler abnormalities, right ventricular overload, or elevated filling pressures — a coexistence of responsiveness and congestion that identifies exactly the patients in whom the risk-benefit balance of a bolus is most uncertain. The evidence here is still maturing. In preload-responsive, fluid-tolerant patients undergoing cardiac surgery, a substantial proportion developed transient venous congestion within minutes of a fluid bolus, and this congestion was associated with worse renal outcomes; remarkably, it could be predicted before fluid administration by the change in portal vein pulsatility index induced by passive leg raising. Yet other studies temper the concept: one multicentre observational study found that fluid challenge did not worsen venous congestion in most fluid responders, suggesting the coexistence may be less common than often assumed. The review also distinguishes left-sided intolerance, marked by pulmonary congestion, elevated E/e’, and B-lines, from right-sided intolerance, marked by systemic venous congestion, right ventricular dilatation, septal dyskinesia, and VExUS abnormalities — phenotypes that frequently coexist but carry different management implications. Acute right ventricular dilatation signals poor fluid tolerance, whereas chronic enlargement from cor pulmonale may represent an adaptive baseline state, making the time course of ventricular change critical to interpretation.

What does this mean at the bedside? The authors propose a pragmatic sequence: first identify the dominant mechanism of shock and rule out major structural or obstructive causes; second, select the appropriate functional test, with passive leg raising plus LVOT VTI as the default when feasible; third, simultaneously assess fluid tolerance using lung ultrasound, right ventricular findings, filling-pressure surrogates, and venous congestion markers; and finally, re-evaluate after each intervention rather than assuming persistent benefit from repeated boluses. When fluid is inappropriate, alternatives exist — optimising vasopressor dosing, adding inotropic support, or, in carefully selected cases, adjusting positive end-expiratory pressure or lightening sedation, though the latter measures are highly context-dependent and can precipitate patient self-inflicted lung injury or pendelluft in patients with existing lung injury. The framework aligns with a broader movement toward stepwise, personalised fluid management rather than automatic repetition of boluses during shock resuscitation.

The honest bottom line is that physiological appeal has so far outrun outcome evidence. Most studies are single-centre, use heterogeneous populations and thresholds, and rely on surrogate haemodynamic endpoints rather than patient-centred outcomes such as mortality, organ failure, or length of stay. No randomised trial has yet shown that an echocardiography-guided approach to fluid therapy improves these outcomes, and operator skill remains a major determinant of reliability — a limitation that tempers enthusiasm for indiscriminate bedside use and reinforces the need for structured training, ideally aligned with the PRICES consensus statement on critical care echocardiography research. Future priorities include outcome-focused trials, standardised training pathways for Doppler-based measurements, and deeper integration of cardiac, lung, and venous ultrasound so that haemodynamic efficacy and congestion are interpreted together rather than in parallel silos. Until that evidence arrives, the review’s central message stands: echocardiographic findings should inform bedside fluid decisions, not dictate them — and the clinically relevant question is no longer simply whether stroke volume can rise, but whether the expected haemodynamic benefit outweighs the risk of pulmonary or systemic congestion.

Subject of Research: Echocardiography-guided fluid resuscitation and fluid tolerance assessment in critically ill adults

Article Title: Echocardiography-guided fluid resuscitation in critical illness: from fluid responsiveness to fluid tolerance

Article References: Attou, R., Jaafari, A., Mansour, S., El Mallouli, M., Redant, S., Gallerani, A., & Khelifa, H. (2026). Echocardiography-guided fluid resuscitation in critical illness: from fluid responsiveness to fluid tolerance. Frontiers in Anesthesiology, 5, Article 1894770. https://doi.org/10.3389/fanes.2026.1894770

Image Credits: AI Generated

DOI: 10.3389/fanes.2026.1894770

Keywords: echocardiography, fluid resuscitation, fluid responsiveness, fluid tolerance, critical care, passive leg raising, LVOT VTI, venous congestion, septic shock, hemodynamic monitoring, intensive care, lung ultrasound